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Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury [endothelial cells]

ABSTRACT: We find that lymphatic Rspo3 is essential for intestinal regeneration after cytotoxic injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE198468 | GEO | 2022/07/18

REPOSITORIES: GEO

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Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury [Rspo3 KO]

Project description:We find that lymphatic Rspo3 is essential for intestinal regeneration after cytotoxic injury.

2022-07-18 | GSE198465 | GEO

Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury [Rspo3 KO]

Project description:Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury [Rspo3 KO]

| PRJNA815348 | ENA

Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury

Project description:Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury

| PRJNA815346 | ENA

Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-18 | GSE198469 | GEO

Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury [endothelial cells]

Project description:Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury [endothelial cells]

| PRJNA815355 | ENA

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [scRNAseq]

Project description:Intestinal stem cells (ISCs) depend on niche factors for proper function. Here, we focus on RSPO3, an essential ISC niche factor, that engages the Lgr5 receptor on ISCs to potentiate WNT signaling, an interaction that is critical for maintaining intestinal stemness. Leveraging novel Rspo3-GFP and Grem1-tdTomato-CreERT2 genetically engineered mice together with single-cell mRNA profiling, we find that RSPO3 is expressed by lymphatic endothelial cells (LECs) and Rspo3+Grem1+ (RG) fibroblasts in the intestinal stroma where RG fibroblasts surround lymphatics and are in close proximity to Lgr5+ ISCs near the crypt base. Functionally, RG fibroblasts through the production of RSPO3 and GREM1 and LECs through the production of RSPO3 foster intestinal organoid propagation in vitro. Rspo3 loss in either or both of these niche cells in vivo compromises ISC numbers, villi length, and repair after irradiation-induced injury. Mechanistically, irradiation-induced damage expands LEC and RG fibroblast numbers and enhances the latters’ generation of RSPO3 through IL-1 receptor activation. We propose that LECs represent a novel component of the ISC niche, which together with RG fibroblasts, provide essential RSPO3 to sustain ISCs in homeostasis and regeneration.

2022-09-08 | GSE185354 | GEO

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200909Yil]

2022-09-08 | GSE185350 | GEO

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200211YilA]

2022-09-08 | GSE185348 | GEO

Aquarius is required for proper CtIP expression and homologous recombination repair.

Project description:Accumulating evidence indicates that transcription is closely related to DNA damage formation and that the loss of RNA biogenesis factors causes genome instability. However, whether such factors are involved in DNA damage responses remains unclear. We focus here on the RNA helicase Aquarius (AQR), a known R-loop processing factor, and show that its depletion in human cells results in the accumulation of DNA damage during S phase, mediated by R-loop formation. We investigated the involvement of Aquarius in DNA damage responses and found that AQR knockdown decreased DNA damage-induced foci formation of Rad51 and replication protein A, suggesting that Aquarius contributes to homologous recombination (HR)-mediated repair of DNA double-strand breaks (DSBs). Interestingly, the protein level of CtIP, a DSB processing factor, was decreased in AQR-knockdown cells. Exogenous expression of Aquarius partially restored CtIP protein level; however, CtIP overproduction did not rescue defective HR in AQR-knockdown cells. In accordance with these data, Aquarius depletion sensitized cells to genotoxic agents. We propose that Aquarius contributes to the maintenance of genomic stability via regulation of HR by CtIP-dependent and -independent pathways.

| S-EPMC5653829 | biostudies-literature

FOXC1 and FOXC2 promote endothelial-derived R-spondin 3 and CXCL12 signals in intestinal regeneration after ischemia-reperfusion injury

Project description:Intestinal ischemia induces mucosal damage while simultaneously activating intestinal stem cells (ISCs), which subsequently regenerate the damaged intestinal epithelium. However, whether angiocrine factors secreted from vascular endothelial cells (ECs) - blood and lymphatic ECs (BECs and LECs, respectively) – regulate ISC-mediated regeneration have yet to be elucidated. Here, we identify FOXC1 and FOXC2 as essential regulators of angiocrine signaling in regeneration of the small intestine after ischemia-reperfusion (I/R) injury. EC- and LEC-specific deletions of Foxc1, Foxc2, or both in mice augment I/R-induced intestinal damage by causing defects in vascular regrowth, expression of the chemokine CXCL12 and the Wnt activator R-spondin 3 in BECs and LECs, respectively, and activation of Wnt signaling in ISCs. Treatment with CXCL12 and R-spondin 3 rescues the I/R-induced intestinal damage in EC- and LEC-Foxc mutant mice, respectively. This study provides evidence that FOXC1 and FOXC2 are required for intestinal regeneration by stimulating angiocrine CXCL12 and Wnt signaling.

2021-12-13 | GSE190581 | GEO

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